The cardioprotective effect of astaxanthin against isoprenaline-induced myocardial injury in rats: Involvement of TLR4/NF-κB signaling pathway
Date
2021
Authors
Journal Title
Journal ISSN
Volume Title
Type
Article
Publisher
Verduci Editore s.r.l
Series Info
European Review for Medical and Pharmacological Sciences.;Volume 25, Issue 11, Pages 4099 - 41052021
Scientific Journal Rankings
Abstract
OBJECTIVE: Cardiovascular diseases (CVDs) are a major cause of morbidity and mortality around the world. Nuclear transcription factor kappa B (NF-κB) represents a factor that plays a major role in the pathogenesis of CVDs. The current study aims to investigate the modulatory effects of astaxanthin and its molecular mechanisms in rats with isoprenaline-induced myocardial infarction. MATERIALS AND METHODS: Rats were pretreated with astaxanthin daily for 14 days prior to inducing myocardial infarction with isoprenaline in the final two days. Blood and heart tissue samples were collected 24 hours after the last dose of isoprenaline was injected for biochemical and histological analysis. RESULTS: Isoprenaline-induced myocardial injury was demonstrated with histopathological examination of heart tissue and the significantly elevated serum troponin-I. Isoprenaline caused an increase in oxidative stress and a decrease in antioxidants. Toll-like receptor-4 (TLR4), NF-κB and tumor necrosis factor-α (TNF-α) expression levels were significantly higher in infarcted rats. Astaxanthin pretreatment had a significant preventive effect on all of the biochemical and molecular parameters tested in myocardial infarcted rats. CONCLUSIONS: Astaxanthin’s cardioprotective effect has been linked to the inhibition of the TLR4/NF-κB signaling pathway. This inhibits the release of inflammatory cytokines, which can cause myocardial cell death. Because of its antioxidant and anti-inflammatory properties, astaxanthin is a promising cardioprotective agent. © 2021 Verduci Editore s.r.l. All rights reserved.
Description
Scopus
Keywords
Astaxanthin, Cardioprotective, Nuclear factor-κβ, Toll like receptor-4, Tumor necrosis factor-α